Premium
Increased sympathetic activity in rats submitted to chronic intermittent hypoxia (CIH) is coupled to enhanced late expiratory activity
Author(s) -
Zoccal Daniel B,
Simms Annabel E,
Bonagamba Leni GH,
Braga Valdir A,
Pickering Anthony E,
Paton Julian FR,
Machado Benedito H
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.739.1
Subject(s) - medicine , brainstem , expiration , respiratory system , control of respiration , carotid body , anesthesia , sympathetic nervous system , endocrinology , blood pressure , carotid arteries
The mechanisms triggering the sympathetic overactivity in CIH rats are not understood. In the present study, we explored whether juvenile rats exposed to CIH exhibit changes in central respiratory‐sympathetic coupling. CIH was induced with 6% O 2 for 40 s every 9 min, 8 h/day for 10 days. On the 11 th day, awake CIH rats breathing room air showed a higher mean arterial pressure than controls (101 ± 3 vs 89 ± 3 mmHg, n = 14). Recordings of phrenic, thoracic sympathetic (tSNA), cervical vagus (cVN) and abdominal nerve (Abd) activities were made in the working heart‐brainstem preparation. During late expiration (Late E), tSNA was greater in CIH (n = 9) than in control rats (52 ± 5 vs 40 ± 3%, n = 11; P < 0.05). Moreover, CIH rats (n = 6), but not controls (n = 5), also exhibited a peak of activity in Abd during Late E with reduced post‐inspiratory activity in cVN. These observations suggest that CIH alters the breathing pattern evoking Late E activity in the Abd. We propose that this Late E discharge in CIH rats contributes with an additional excitatory synaptic drive to the sympathetic outflow and, in turn, raises arterial pressure. Further studies are required to identify the neuronal populations and the correspondent neurochemical mechanisms responsible for the altered respiratory‐sympathetic entrainment in CIH rats. Supported by CNPq and FAPESP (Brazil) and BHF (UK).